[Noise in intensive care units. Do the alarms for subspecialties differ]. / Lärm auf der Intensivstation: Unterscheiden sich die Alarme in den Fachdisziplinen?

INTRODUCTION: Cardiovascular monitoring alarms are frequent in intensive care units (ICUs) and lead to noise levels often exceeding 80 dB. The aim of this study was to evaluate if there are relevant differences between ICUs with different subspecialties in the frequency and distribution of alarm signals, their occurrence during the day, the types of alarms and the underlying vital parameters. METHODS: All alarm signals of the cardiovascular monitoring systems from randomly chosen patients at five different ICUs of the university hospital of Regensburg were evaluated. RESULTS: No significant differences between the ICUs regarding the frequency of alarm signals and only slight differences in the time distribution could be recognized (p=0.02). The most frequent alarm signals were from threshold alarms (61%) followed by technical alarms. The majority of alarms generated were related to invasive arterial blood pressure measurement. CONCLUSIONS: The frequency and distribution of ICU alarm signals seem to be comparable on different ICUs. Therefore, implementation of universal concepts for alarm reduction seems to be applicable regardless of the subspecialty of the ICU.

[Myocardial lactate extraction during programmed ventricular stimulation and its value for etiologically-related therapy of ischemic ventricular tachyarrhythmia]. / Myokardiale Laktatextraktion während programmierter Ventrikelstimulation und ihre Bedeutung für die Kausaltherapie ischämisch induzierter ventrikulärer Tachyarrhythmien.

UNLABELLED: Ischemia is considered to be one of the most important trigger mechanisms of ventricular tachyarrhythmias, i.e., tachycardia (VT) and fibrillation (VF) in coronary artery disease (CAD). The aim of the study was 1) to investigate the relationship between ischemia and inducibility of VT/VF, and 2) to address the question, if removal of ischemia leads to suppression, resp. noninducibility of arrhythmias. In 30 patients (pts) with CAD (healed myocardial infarction in 73%, acute myocardial infarction excluded) and sustained malignant ventricular arrhythmias (VF in 47%, VT in 37%, and arrhythmogenic syncope in 16%) the myocardial lactate extraction (MLE) was calculated by measuring the arterio venous coronary lactate difference simultaneously during programmed ventricular stimulation. Eighteen pts (group A, "lactate-positive") showed a significant decrease of MLE from +16 +/- 13% at rest to -18 +/- 24% during stimulation just before induction of VT/VF (p < 0.0005). During recovery up to 10 min following termination of VT/VF MLE returned to normal range (+19 +/- 16%). In 12 pts (group B, "lactate-negative") MLE showed no significant change between rest, stimulation, and recovery. Compared to group B pts, group A pts demonstrated a significantly higher number and degree of coronary lesions as well as regions with reversible ischemia during 201Tl- scintigraphy. Lactate-positive pts presented spontaneous arrhythmias of higher frequency and had usually a two- or three-vessel disease, while lactate-negative pts presented arrhythmias of lower frequency and had more often a one-vessel disease with ventricular aneurysm. 17/18 (94%) group A pts underwent coronary bypass grafting (11) or balloon angioplasty (6) and were rendered noninducible during post interventional PVS in 94%, showing also a normalized MLE in 87% of cases. In group B only 4/12 pts were suitable for revascularization and could be rendered noninducible in only 50% of cases. With respect to the success-rate of the anti-ischemic therapy in terms of arrhythmia suppression, a lactate-positive result during primary PVS had a sensitivity of 89%, a specificity of 75%, a positive predictive value of 94%, and a negative predictive value of 60%. IN CONCLUSION: in about 60% of pts with VT/VF and significant CAD a correlation between ischemia and inducibility could be demonstrated. MLE during PVS has a highly significant predictive value for the effect of an antiischemic intervention on arrhythmia induction.

Defibrillation energy requirements with single endocardial (Endotak) lead.

The need for thoracotomy in usually high risk patients has limited the use of the implantable cardioverter defibrillator. Initial clinical results with endocardial and subcutaneous patch electrodes (SQPs) are encouraging. Using a single endocardial lead in the absence of a SQP for chronic implantation of the cardioverter defibrillator, the goal of the study was to obtain defibrillation thresholds (DFTs) of 15 Joules (J) or less and to investigate changes in DFT over time. We tested 19 consecutive patients (15 men, 4 women) age 62 +/- 8.5 years with malignant ventricular arrhythmias (14 VT/5 VF). The underlying heart disease was coronary artery disease in 15 patients, dilative cardiomyopathy in two patients, and primary electrical disease in two patients. Four patients had undergone previous cardiac surgery. Left ventricular ejection fraction ranged between 14% and 66% (39% +/- 12.6%). Pacing thresholds (0.54 +/- 0.17 V at 0.5 msec), R wave amplitude for pacemaker sensing (14.2 +/- 7.0 mV), slew rate (2.12 +/- 1.4 V/sec), and resistance (500.3 +/- 73.9 W) were sufficient in all patients. Eighteen patients met our endocardial implant criteria with a DFT < or = 15 J (10.05 +/- 4.03 J) using monophasic (14 patients) or biphasic (four patients) pulse wave forms. In the one remaining patient, with a DFT of 20 J, we implanted a SQP but there was no reduction of the DFT. All patients tested showed successful defibrillation prior to discharge. During follow-up of 88 patient-months (1-9 months), 114 spontaneous VT/VF episodes occurred in five patients and were all successfully terminated. Eleven patients with a minimum follow-up of 2 months were reassessed.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiological and therapeutic implications of cardiac arrhythmias in hypertension.

UNLABELLED: Hypertension, especially if associated with left ventricular hypertrophy (LVH), is a risk factor in complex ventricular arrhythmia (VA) and sudden cardiac death (SCD). To determine the effectiveness of the clinical use of programmed ventricular stimulation (PVS) we studied 40 symptomatic hypertensive patients after excluding coronary heart disease (CHD), as characterized by dizziness and palpitation, syncope, aborted SCD and/or documented complex VA. PVS revealed a normal result, i.e. a maximum of six ventricular echobeats, in 70% (group A) and a pathological result, i.e. ventricular tachycardia (VT) or fibrillation (VF) in 30% (group B). Both groups differed significantly with respect to LV (left ventricular) muscle mass: 158 +/- 45 (A) vs. 222 +/- 112 (B) g.m-2, LVEF (left ventricular ejection fraction): 71 +/- 17% (A) vs. 47 +/- 18% (B) and LV end-systolic volume index: 34 +/- 25 (A) vs. 63 +/- 27 (B) ml.m-2. Coronary reserve was comparably reduced in both groups: 2.6 +/- 1.0 (A) vs. 2.3 +/- 0.6 (B). In 3/8 (37%) patients with aborted SCD and VT/VF the clinical VA (2/2 VT and 1/6 VF) could be induced, whereas in the remaining five patients nsVT or no complex VA was induced. The therapeutic regimen included no drugs in 30%, beta-blockers in 50%, serial drug testing in 12% and implantation of an automatic cardioverter defibrillator (AICD) in 8% of patients. Ventricular late potentials (LPs), detected by the signal averaging electrocardiogram, represent zones of delayed myocardial activation, which may become an origin of ventricular tachycardias. Three criteria constitute a positive LP: (1) QRS duration greater than 114 ms, (2) root mean square voltage of the last 40 ms less than 20 microV and (3) duration of low amplitude signal below 40 microV greater than 38 ms. To look for the prognostic value of LP in hypertension we investigated 43 hypertensive patients without evidence of CHD. All three criteria were positive in 4/43 patients (9%), three of them demonstrating inducible monomorphic VT during PVS. 17/30 patients (56%) with LVH had at least one positive criterion, whereas only one out of 13 patients without left ventricular hypertrophy (8%) had one positive criterion. Symptomatic patients presenting with syncope, aborted SCD or documented VT/VF differed significantly from patients without symptoms or complex arrhythmias in regard to all three criteria. CONCLUSION: In hypertensive heart disease clinical arrhythmias as well as the result of electrophysiological testing are closely related to left ventricular performance and hypertrophy.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of aldosterone on intralymphocytic sodium and potassium in patients with essential hypertension.

In vitro binding of aldosterone to mineralocorticoid receptors on human mononuclear leukocytes (HML) and its effects on the intracellular sodium and potassium concentrations of HML have already been described. In the present paper this easily accessible human cell model was investigated in 13 patients with essential hypertension. In only four patients sodium in HML without incubation was elevated compared with the range for normal persons. A decrease of intracellular sodium or potassium occurred during incubation without aldosterone (P less than 0.02). The addition of 1.4 nM aldosterone did not prevent this loss of electrolytes as observed in normal persons. Plasma renin activity and aldosterone were not correlated with the electrolyte response and were within the normal limits. The number of mineralocorticoid receptors/cell were within or close to the normal range (n = 9). The independence of intracellular electrolytes from aldosterone despite a normal number of mineralocorticoid receptors may reflect an impairment of the mineralocorticoid effector mechanism in the HML of patients with essential hypertension.

Volume regulation of human lymphocytes by aldosterone in isotonic media.

In vitro binding of aldosterone to mineralocorticoid receptors on human mononuclear leukocytes (HML) and its effects on the intracellular sodium and potassium concentrations of HML have already been described. In the present paper this easily accessible human cell model was investigated with regard to the regulation of the cell volume by aldosterone, since the concordant changes of sodium and potassium were expected to be accompanied by water and volume shifts. As determined by the measurement of cell diameter and the planimetric estimation of cell area in photographs, cell volume decreased by approximately 16% when cells were incubated in RPMI-1640 medium without aldosterone added for 1 h at 37 degrees C, a decrease not seen when 1.4 nM aldosterone was added to the incubation medium; the effect was half maximal at a concentration between 0.07 and 0.14 nM. One hundred forty nanomoles canrenone antagonized the action of aldosterone, but cortisol was ineffective. The results indicate concordant changes of intracellular sodium and potassium and cell volume, if studied under the same conditions. These data are the first to demonstrate that aldosterone is a major physiological determinant of lymphocyte volume in isotonic media.

Effects of aldosterone on intralymphocytic sodium and potassium in patients with primary aldosteronism.

In vitro effects of aldosterone have been described with regard to the intracellular sodium and potassium concentrations of human mononuclear leukocytes. In the present paper the in vitro effect of aldosterone on the intracellular sodium and potassium of human mononuclear leukocytes in 6 patients with primary aldosteronism was investigated. Except for one patient with elevated intracellular electrolytes, sodium and potassium in mononuclear leukocytes of patients with aldosteronism without incubation were within the range for normals. In the patients, no significant change of intracellular sodium or potassium was observed during incubation with or without aldosterone (1.4 nmol/l), whereas in normals, the loss of sodium and potassium during incubation without aldosterone was prevented by 1.4 nmol/l aldosterone. This insensitivity to aldosterone indicates that intracellular electrolytes in mononuclear leukocytes of patients with primary aldosteronism are kept in normal ranges by mechanism which are independent of mineralocorticoids and may represent the cellular correlate to the renal 'escape' phenomenon in aldosteronism.